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Epithelial Cell-Derived IL-25, but Not Th17 Cell-Derived IL-17 or IL-17F, Is Crucial for Murine Asthma
Citation
Suzukawa, M and Morita, H and Nambu, A and Arae, K and Shimura, E and Shibui, A and Yamaguchi, S and Suzukawa, K and Nakanishi, W and Oboki, K and Kajiwara, N and Ohno, T and Ishii, A and Korner, H and Cua, DJ and Suto, H and Yoshimoto, T and Iwakura, Y and Yamasoba, T and Ohta, K and Sudo, K and Saito, H and Okumura, K and Broide, DH and Matsumoto, K and Nakae, S, Epithelial Cell-Derived IL-25, but Not Th17 Cell-Derived IL-17 or IL-17F, Is Crucial for Murine Asthma, Journal of Immunology, 189, (7) pp. 3641-3652. ISSN 0022-1767 (2012) [Refereed Article]
Copyright Statement
Copyright 2012 The American Association of Immunologists
DOI: doi:10.4049/jimmunol.1200461
Abstract
IL-17A, IL-17F, and IL-25 are ligands for IL-17RA. In the current study, we demonstrated that IL-25-deficient mice-but not IL-17A-, IL-17F-, IL-17A/F-, IL-23p19-, or retinoic acid-related orphan receptor (ROR)-γt-deficient mice-showed significant suppression of 1) the number of eosinophils and the levels of proinflammatory mediators in bronchoalveolar lavage fluids, 2) airway hyperresponsiveness to methacholine, and 3) OVA-specific IgG1 and IgE levels in the serum during OVA-induced Th2-type/eosinophilic airway inflammation. The IL-25 deficiency did not affect lung dendritic cell migration or Ag-specific memory-Th2 cell expansion during Ag sensitization. Adoptive transfer of T cells, mast cells, or bone marrow cells from IL-25-deficient mice revealed that induction of Th2-type/eosinophilic airway inflammation was dependent on activation of lung epithelial cells and eosinophils by IL-25 produced by airway structural cells such as epithelial cells but not by such hematopoietic stem-cell-origin immune cells as T cells and mast cells. Therefore, airway structural cell-derived IL-25-rather than Th17 cell-derived IL-17A and IL-17F-is responsible for induction of local inflammation by promoting activation of lung epithelial cells and eosinophils in the elicitation phase of Th2-type/eosinophilic airway inflammation. It is not required for Ag-specific Th2 cell differentiation in the sensitization phase.
Item Details
| Item Type: | Refereed Article |
|---|---|
| Research Division: | Medical and Health Sciences |
| Research Group: | Immunology |
| Research Field: | Immunology not elsewhere classified |
| Objective Division: | Expanding Knowledge |
| Objective Group: | Expanding Knowledge |
| Objective Field: | Expanding Knowledge in the Medical and Health Sciences |
| Author: | Korner, H (Professor Heinrich Korner) |
| ID Code: | 80705 |
| Year Published: | 2012 |
| Web of Science® Times Cited: | 51 |
| Deposited By: | Menzies Institute for Medical Research |
| Deposited On: | 2012-11-08 |
| Last Modified: | 2013-07-02 |
| Downloads: | 0 |
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